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Each year, approximately 750, 000 to 850, 000 teenage women in the United States experience pregnancy.10, 11 Seventy-four to 95 percent of teen pregnancies are unintended.12, 13 In 1999, the estimated U.S. teen pregnancy rate was 87 pregnancies per 1, 000 females ages 15 to 19--a drop of 25 percent from the 1990 rate of 116.14, 15 [Note: 1999 is the most recent year for which published pregnancy data is available.] Some researchers attribute 75 percent of the decline in U.S. teen pregnancy rates to better contraceptive use among sexually experienced teens and 25 percent of the decrease to increased abstinence; others credit the two factors about equally.5, 15.
RESULTS In vitro antimicrobial activity. Table 1 shows the MICs of benzoxazinorifamycins for 50% MlC50 ; and 90% MIC90 ; of the various mycobacterial strains. All the drugs KRM-1648, KRM-1657, KRM-1668, KRM-1686, and KRM-1687 ; had much smaller MICs than RMP, in particular those drugs active against slowly growing mycobacteria, such as M. tuberculosis especially RMP-susceptible strains ; , M. kansasii, M. marinum, M. scrofulaceum, M. avium, and M. intracellulare 8 to 512 times lower than the M'C50 of RMP and 8 to 128 times lower than the MIC90 of RMP ; . In contrast, the MICs of the drugs against rapidly growing mycobacteria, such as M. fortuitum, M. chelonae subsp. abscessus, and M. chelonae subsp. chelonae, were not reduced in such a marked manner by these benzoxazinorifamycins compared with that of RMP, and the drugs were virtually inactive against these organisms. Among the drugs tested, KRM-1648 exhibited the strongest antimicrobial activity, followed by KRM-1657, although this was true only for slowly growing mycobacteria. However, it was noted that the activity of KRM-1648 against RMP-resistant strains of M. tuberculosis was considerably lower than those of other KRMs, although KRM-1648 exhibited the most potent activity against RMP-susceptible strains of M. tuberculosis. Figure 2 compares cumulative susceptibilities of various species of slowly growing mycobacteria to KRM-1648, KRM-1657, and RMP. This analysis also shows remarkable superiority of the two benzoxazinorifamycins in terms of in vitro antimycobacterial activities when compared with that of RMP. It is noteworthy that the benzoxazinorifamycins had a much more narrow range of MIC distribution in terms of log concentration ; in M. tuberculosis, M. kansasii, M. marinum, and M. scrofulaceum. On the other hand, the benzoxozinorifamycins had nearly the same range of MIC distribufion for M. intracellulare as did RMP and had a much wider range of MIC distribution than did RMP against M. avium. Further, it may be noted that in the test strains of M. avium, there was a small number of organisms highly resistant to the two KRMs MIC, -100 jig ml ; , whereas such a phenomenon was not observed in other mycobacterial species. The other three benzoxazinorifamycins KRM-1668, KRM-1686, and KRM-1687 ; had MIC distribution patterns similar to those, of KRM-1648 and KRM-1657 data not shown ; . Activity against intracellular organisms. Table 2 shows the activities of benzoxazinorifamycins against M. intracellulare N-260 phagocytosed in murine peritoneal macrophages. MICs of the drugs against M. intracellulare N-260 were as follows in micrograms per milliliter ; : KRM-1648, 0.05; KRM-1657, 0.1; KRM-1668, 0.2; KRM-1686, 0.1; KRM1687, 0.1; RMP, 12.5; and RBT, 0.4. When these drugs were.
Murine models of gvhd
SOD1ADIS plays a crucial role in the pathogenesis of mutant SOD1-mediated ALS. This finding may provide a therapeutic target for ALS. Mutations in SOD1 gene are responsible for 20% of familial ALS cases. Scientists in the Les Turner Laboratory previously identified a mutation in the SOD1 gene, called A4V, which accounts for approximately 50% of the SOD1-ALS cases within North America. This same A4V mutation is rare in Europe. That led the scientists to wonder whether there could have been an original source of the AV mutation in North America, something called a founder effect. Dr. Mohammad Saeed and his team tested to see if a founder effect contributes to such a high prevalence of A4V in North America. Their data suggest the North America A4V mutation descended from two founders European and Amerindian ; 400500 years ago. Ten genetic loci have been identified for familial ALS. Whether a person's genetic background contributes to development of.
22. 1. Loftus, S. K., J. A. Morris, E. D. Carstea, J. Z. Gu, C. Cummings, A. Brown, J. Ellison, K. Ohno, M. A. Rosenfeld, D. A. Tagle, et al. 1997. Murine model of Niemann-Pick C disease: mutation in a cholesterol homeostasis gene. Science. 277: 232235. 2. Carstea, E. D., J. A. Morris, K. G. Coleman, S. K. Loftus, D. Zhang, C. Cummings, J. Gu, M. A. Rosenfeld, W. J. Pavan, D. B. Krizman, et al. 1997. Niemann-Pick C1 disease gene: homology to mediators of cholesterol homeostasis. Science. 277: 228231. 3. Naureckiene, S., D. E. Sleat, H. Lackland, A. Fensom, M. T. Vanier, R. Wattiaux, M. Jadot, and P. Lobel. 2000. Identification of HE1 as the second gene of Niemann-Pick C disease. Science. 290: 22982301. 4. Xie, C., S. D. Turley, P. G. Pentchev, and J. M. Dietschy. 1999. Cholesterol balance and metabolism in mice with loss of function of Niemann-Pick C protein. Am. J. Physiol. 276: E336E344. 5. Vanier, M. T., and G. Millat. 2003. Niemann-Pick disease type C. Clin. Genet. 64: 269281. 6. Millat, G., K. Chikh, S. Naureckiene, D. E. Sleat, A. H. Fensom, K. Higaki, M. Elleder, P. Lobel, and M. T. Vanier. 2001. NiemannPick disease type C: spectrum of HE1 mutations and genotype phenotype correlations in the NPC2 group. Am. J. Hum. Genet. 69: 10131021. 7. Sevin, M., G. Lesca, N. Bauman, G. Millat, O. Lyon-Caen, M. T. Vanier, and F. Sedel. 2006. The adult form of Niemann-Pick disease type C. Brain. 260: 114. 8. Mieli-Vergani, G., E. R. Howard, and A. P. Mowat. 1991. Liver disease in infancy: a 20 year perspective. Gut. Suppl. ; : 123128. 9. Kelly, D. A., B. Portmann, A. P. Mowat, S. Sherlock, and B. D. Lake. 1993. Niemann-Pick disease type C: diagnosis and outcome in children, with particular reference to liver disease. J. Pediatr. 123: 242247. 10. Yerushalmi, B., R. J. Sokol, M. R. Narkewicz, D. Smith, J. W. Ashmead, and D. A. Wenger. 2002. Niemann-Pick disease type C in neonatal cholestasis at a North American center. J. Pediatr. Gastroenterol. Nutr. 35: 4450. 11. Birch, N. C., S. Radio, and S. Horslen. 2003. Metastatic hepatocellular carcinoma in a patient with Niemann-Pick disease, type C. J. Pediatr. Gastroenterol. Nutr. 37: 624626. 12. Nicholson, A. G., R. Florio, D. M. Hansell, R. M. du Bois, A. U. Wells, P. Hughes, H. K. Ramadan, C. I. Mackinlay, E. Brambilla, G. R. Ferretti, et al. 2006. Pulmonary involvement by Niemann-Pick disease. A report of six cases. Histopathology. 48: 596603. 13. Palmeri, S., P. Tarugi, F. Sicurelli, R. Buccoliero, A. Malandrini, M. M. De Santi, G. Marciano, C. Battisti, M. T. Dotti, S. Calandra, et al. 2005. Lung involvement in Niemann-Pick disease type C1: improvement with bronchoalveolar lavage. Neurol. Sci. 26: 171173. 14. Uyan, Z. S., B. Karadag, R. Ersu, G. Kiyan, E. Kotiloglu, S. Sirvanci, F. Ercan, T. Dagli, F. Karakoc, and E. Dagli. 2005. Early pulmonary involvement in Niemann-Pick type B disease: lung lavage is not useful. Pediatr. Pulmonol. 40: 169172. 15. Pin, I., S. Pradines, O. Pincemaille, P. Frappat, E. Brambilla, M. T. Vanier, and M. Bost. 1990. Forme respiratoire mortelle de maladie de Niemann-Pick type C. Arch. Fr. Pediatr. 47: 373375. 16. Pentchev, P. G., M. T. Vanier, K. Suzuki, and M. C. Patterson. 1995. Niemann-Pick disease type C: a cellular cholesterol lipidosis. In The Metabolic and Molecular Bases of Inherited Diseases. C. R. Scriver, 23.
Murine macrophage cell line
Presenters: Charles Kerr and Stuart Connolly, McMaster University, Hamilton, Ontario, Canada. The study: A randomized trial of physiological pacemakers versus single-chamber VVI pacemaker in 2568 patients requiring ventricular pacing. The primary end point of the trial was the incidence of cardiovascular death or stroke. The results: Preliminary results indicate that at a mean follow-up of 3.1 years, the incidence of cardiovascular death or stroke was 4.78% per year in the physiological pacing group and 5.43% per year in the VVI pacing group, a nonsignificant difference. The event curves appeared to overlap for the first 2 years of follow-up, and then some divergence of the curves was apparent. There were no significant differences between groups in 6-minute walk test performance or the incidence of CHF. The physiological pacing group was noted to have a somewhat lower incidence of atrial fibrillation AF ; 5.34% per year versus 6.59% per year again, these differences appeared to emerge after 2 years. Summary: In the overall CTOPP population, physiological pacing did not appear to result in symptomatic benefit. Further extended follow-up and subgroup analyses will help clarify these results.
Gesterone recognition sequence 26 ; . The murine gene, which is better characterized 8, 13 ; , also has putative estrogen, glucocorticoid, and progesterone response elements that enable these steroids to exert transcriptional control on OPN expression in mouse tissues. Presumably, progesterone exerts its stimulatory effect on OPN expression by its action on the promoter region in the human gene. The observation of a partial agonistic activity of RU486 in the trophoblasts suggests binding of RU486-receptor complexes to the OPN promoter, which is additional evidence for the presence of a putative progesterone response element in the upstream region of the OPN gene. Although the full functional significance of the presence of OPN in the chorionic villus remains to be determined, its actions in other cell systems suggest a potential role for this matrix protein in the regulation of important processes of the placenta. It has been shown that OPN can function as a cytokine and that it can exert a chemoattractant effect on macrophages and stimulate IgM and IgG antibody production by B cells 27 ; . In addition, T cell activation by OPN has also been reported 28 ; . Likewise, recent work indicates a role for OPN in nitric oxide synthesis 29 ; , a process of potential significance in the course of normal placentation and placental function. Thus, abnormalities in the regulation of expression of OPN by human cytotrophoblasts and its action s ; on surrounding tissues may be related to the development of complications of pregnancy that are associated with altered nitric oxide synthase activity, such as preeclampsia. It has also been shown that OPN inhibits urinary calculi formation 5 ; , thus making it conceivable that it may help to prevent calcifications of the placenta. In addition, we propose that one of the critical roles of OPN in the placenta may be in the regulation of syncytiotrophoblast function. OPN's main known receptors are members of the v family of integrins 30 ; , and the binding of OPN to its integrin receptors mediates several processes, including cell adhesion and signaling. It has been demonstrated that the v 3 integrin is expressed by human syncytiotrophoblasts, but not by mononuclear cytotrophoblasts 31 ; . Further, some of our recent findings demonstrate that human trophoblasts attach to OPN and that this adhesion is mediated at least in part by the v 3 integrin 32 ; . Preliminary results indicate that binding of OPN to syncytiotrophoblasts generates intracellular calcium oscillations, indicating a role for this molecule in trophoblast signaling Coutifaris, C., unpublished observations ; . Thus, we propose that in vivo, the OPN synthesized and secreted by mononuclear cytotrophoblasts binds to v integrins, i.e. v 3, present in the overlying syncytiotrophoblast facilitating adhesion and communication between the two cell layers see schematic representation in Fig. 6 ; . We postulate that this adhesive and or signaling event is vital for maintaining the structural integrity of the chorionic villus and has an as yet uncharacterized role in the normal function of the syncytiotrophoblast. In this study we have demonstrated a novel regulatory feedback system between the trophoblast syncytium and the underlying cytotrophoblast cell layer: secretion of progesterone by the target cell the syncytiotrophoblast ; regulates the expression of OPN the paracrine factor ; by the underlying mononuclear cytotrophoblast. OPN, in turn, can then and muse.
Murine for your eyes
FIG. 3. Tissue distribution of Cnt3 mRNA in male and female rats and mice. Ten micrograms of total RNA from various tissues of male and female Sprague-Dawley rats or C57BL 6 mice were analyzed with the Cnt3-specific probe set described under Materials and Methods. The y-axis represents the RLU per 10 g of total tissue RNA. Data represent mean standard error of determinations from five samples per group, except the data on pituitary rats and mice ; and ovary mice ; , which are the mean of duplicate pooled pituitary or ovary samples from 10 rats or mice. Liv, liver; Kid, kidney; Lun, lung; Sto, stomach; Duo, duodenum; Jej, jejunum; Ile, ileum; L.I., large intestine; Brn, brain; Pit, pituitary; Ht, heart; Thy, thymus; Spl, spleen; Mus, skeletal muscle; B.V., blood vessels; Gon, gonads; Pro, prostate; Ute, uterus. ND, not determined. , p 0.05 compared with males.
Murine macrophage cell lines
Effects of Mevinolin on Incorporationof Labeled Precursors into Ubiquinone-To study the effects of mevinolin on ubiquinone synthesis in cultured neuroblastoma cells, we used ["]acetate or [l4C]acetate as precursors for the isoprenoid of chain and [14C]tyrosineas a precursor for the quinone ring the molecule. Acetate was preferred over mevalonate as an isoprenoid precursor because competitive inhibitorsof HMGCoA reductase apparently decrease the size of the intracellular 0 FA 40 mevalonate pool, thereby causing an increase in thelabeling of ubiquinone with [3H]mevalonate which probably reflects an increase in the specific radioactivity of the intracellular mevalonate pool, rather than a true increase in the rate of ubiquinonesynthesis 11-13 ; . However, because acetate is incorporated into non-isoprenoid lipids, it was necessary to O7 `b use a two-dimensional thin-layer chromatography system to ensure complete separation of ubiquinone from other lipids Fig. la ; . When cells were incubated with [I4C]acetate, the labeled material that co-migrated with authentic ubiquinone on the two-dimensional chromatogram yielded a single band FIG. 1. Isolation of ubiquinone by thin-layer chromatograof radioactivity when eluted and rechromatographed on conphy. a, two-dimensional thin-layer chromatogram illustratinga typventional silica gel plates using a third solvent system Fig. ical separation of lipid standards see "Experimental Procedures" for lb ; . Therewas no indication of contamination of ubiquinone details ; . PL, phosphatidylcholine + sphingomyelin; MG, monolein; with dolichol or free fatty acids, the lipids nearest to ubiqui- 1, 2-DG, 1, C, cholesterol; L, lanosterol; none on the two-dimensional chromatogram. However, since D, dolichol; FA, oleic acid; Qlo, ubiquinone-10; TG, triolein; S, squalene; CE, cholesteryl oleate. Lipids were visualized by spraying the ubiquinone-10 and ubiquinone-9 migrate together on convenplate with 50% H2S0, . The mobilities of the lipid standards were not tional thin-layer plates, we also subjected the [14C]acetatealtered substantiallywhen they were mixed with lipidsextracted from labeled material to reverse-phase thin-layer chromatography cultured cells. b, cultured neuroblastoma cells were incubated with in a system capable of separating ubiquinonespecies accord- ["Clacetate 4 pCi mlof medium ; for 24 h, and the material coing to the length the isoprenoid chain Fig. IC ; . of The results migrating with ubiquinone-10 on thetwo-dimensional chromatogram a silica gel plate indicated that approximately90% of the radioactive product see a ; was elutedandrechromatographedon synthesized by the murine neuroblastoma cells was ubiqui- developed with methylene chloride ethyl acetate 97: 3, v v ; . The the labeled material relative to the standards was deternone-9. In this respect the mouse neuroblastoma cells are position ofautoradiography. c, the ["Clacetate-labeled material comined by similar to rat tissues 33-36 ; and differ from human fibro- migrating with ubiquinone-10 in the conventional thin-layer chroblasts, whereubiquinone-10 predominates 11 ; . Chromato- matography systems shown above a and b ; was subjected to reversegraphic analysis usingubiquinone-6 and ubiquinone-7as car- phasechromatography see"ExperimentalProcedures" ; , andthe position of the labeled material was visualized by autoradiography. riers in the two-dimensional and reverse-phase systems showed no detectable incorporation labeled acetate into the When thezones containing theubiquinone-9 and ubiquinone-10 were of scraped and counted, the ubiquinone-9 spot contained 88.2% of the short-chain ubiquinone species data not shown ; . In the reradioactivity 14, 785 dpm ; compared to 11.8% 1, 979 dpm ; in the verse-phase system there was evidence of rapidly migrating ubiquinone-10. no isoprenoids, such as squalene dioxides, which have been reported to co-migrate with ubiquinone in some conventional inhibition of ubiquinone synthesiswas observed a t mevinolin chromatography systems 28 ; . concentrations above 10 pM. The suppression of ubiquinone To assess the effectsof mevinolin on de novo synthesis of ubiquinone in neuroblastoma cells, we measured the incor- synthesis by 25 mevinolin was apparent by 1 h after poration of [3H]acetate into ubiquinone in cells that were addition of the inhibitor, and was demonstrable with ["C] I ; . exposed to various concentrations of the reductase inhibitor tyrosine as well as with [3H]acetate Table Effects of Blocking Mevalonute Synthesis on Mitochondrial for 24 h Fig. 2 ; . To control for possible nonspecific effects of mevinolin on acetate uptake or the size of the intracellular Ubiquinone Content-When ubiquinone was measured in miacetyl-coA pool, we also measured the incorporationof [3H] tochondrial extracts from cells that had been exposed to 25 of acetate into fatty acids in the same cultures 2 ; . Maximum p~ mevinolinfor 24 h, we found thattheinhibition Fig and mycostatin.
Endemic murine typhus disease
25. Attie, A.D. 2004 ; The mystery of PCSK9. Arterioscler. Thromb. Vasc. Biol., 24, 13371339. 26. Jirholt, P., Adiels, M. and Boren, J. 2004 ; How does mutant proprotein convertase neural apoptosis-regulated convertase 1 induce autosomal dominant hypercholesterolemia? Arterioscler. Thromb. Vasc. Biol., 24, 13341336. 27. Boren, J., Rustaeus, S. and Olofsson, S.O. 1994 ; Studies on the assembly of apolipoprotein B-100- and B-48-containing very low density lipoproteins in McA-RH7777 cells. J. Biol. Chem., 269, 2587925888. 28. Sun, X.M., Patel, D.D., Knight, B.L. and Soutar, A.K. 1998 ; Influence of genotype at the low density lipoprotein LDL ; receptor gene locus on the clinical phenotype and response to lipid-lowering drug therapy in heterozygous familial hypercholesterolaemia. The Familial Hypercholesterolaemia Regression Study Group. Atherosclerosis, 136, 175185. 29. O'Neill, F.H., Patel, D.D., Knight, B.L., Neuwirth, C.K., Bourbon, M., Soutar, A.K., Taylor, G.W., Thompson, G.R. and Naoumova, R.P. 2001 ; Determinants of variable response to statin treatment in patients with refractory familial hypercholesterolemia. Arterioscler. Thromb. Vasc. Biol., 21, 832837. 30. Benjannet, S., Rhainds, D., Essalmani, R., Mayne, J., Wickham, L., Jin, W., Asselin, M.C., Hamelin, J., Varret, M., Allard, D. et al. 2004 ; NARC-1 PCSK9 and its natural mutants: zymogen cleavage and effects on the LDLR and LDL-cholesterol. J. Biol. Chem., 279, 48865 48875. Mayer, M., Kies, U., Kammermeier, R. and Buchner, J. 2000 ; BiP and PDI cooperate in the oxidative folding of antibodies in vitro. J. Biol. Chem., 275, 2942129425. 32. Nakamura, N., Lowe, M., Levine, T.P., Rabouille, C. and Warren, G. 1997 ; The vesicle docking protein p115 binds GM130, a cis-Golgi matrix protein, in a mitotically regulated manner. Cell, 89, 445455. 33. Wang, A.B., Liu, D.P. and Liang, C.C. 2003 ; Regulation of human apolipoprotein B gene expression at multiple levels. Exp. Cell Res., 290, 112. 34. Fisher, E.A., Zhou, M., Mitchell, D.M., Wu, X., Omura, S., Wang, H., Goldberg, A.L. and Ginsberg, H.N. 1997 ; The degradation of apolipoprotein B100 is mediated by the ubiquitinproteasome pathway and involves heat shock protein 70. J. Biol. Chem., 272, 2042720434. 35. Bissonnette, L., Charest, G., Longpre, J.M., Lavigne, P. and Leduc, R. 2004 ; Identification of furin pro-region determinants involved in folding and activation. Biochem. J., 379, 757 763. Cardozo, C., Wu, X., Pan, M., Wang, H. and Fisher, E.A. 2002 ; The inhibition of microsomal triglyceride transfer protein activity in rat hepatoma cells promotes proteasomal and nonproteasomal degradation of apoprotein B100. Biochemistry, 41, 1010510114. 37. Leiper, J.M., Bayliss, J.D., Pease, R.J., Brett, D.J., Scott, J. and Shoulders, C.C. 1994 ; Microsomal triglyceride transfer protein, the abetalipoproteinemia gene product, mediates the secretion of apolipoprotein B-containing lipoproteins from heterologous cells. J. Biol. Chem., 269, 2195121954. 38. Burden, J.J., Sun, X.M., Garcia Garcia, A.B. and Soutar, A.K. 2004 ; Sorting motifs in the intracellular domain of the low density lipoprotein LDL ; receptor interact with a novel domain of sorting nexin-17. J. Biol. Chem., 279, 1623716245.
Murine cells wikipedia
Taketh unto him seven other spirits worse then himself, and so enter they in and dwell there. And the end of that man is worse than the beginning. Even so shall it be with this evil nation. While he yet talked to the people: behold his mother and his brethren stood without, desiring to speak with him. Then one said unto him: behold thy mother and thy brethren stand without, desiring to speak with thee. He answered and said to him that told him: Who is my mother? or who are my brethren? And he stretched forth his hand over his disciples and said: behold my mother and my brethren. For whosoever doth my fathers will which is in heaven, the same is my brother, sister and mother and mysoline.
| Murine tsui agencyNMR OF TNF-TREATED Table 2 Effect of TNF on Ihe concentrations pmol g wet weight of tissue ; of water-soluble phospholipid metabolites in tissue extracts of3CI-8 FLC tumors DBA 2 mice were injected s.c. with 5 x 10 * FLC clone 3CI-8 ; . Five tumor samples were dissected on day 14 of tumor growth, 6 h after treatment with 0.2 ml of murine TNF 20 ml in NaCI 153 mM buffered saline containing BSA, 100 ig ml ; .Five control tumors were treated with BSA 100 g ml ; . Tumor extracts in EtOH: H2O 60: 40, v v ; were prepared from the two respective pools of tumors frozen immediately after dissection at liquid nitrogen temperature. Quantitative determinations of the average concentrations of GroP, PEtn, PCho, GroPCho, and GroPEtn were made on the basis of a combined analysis of the "P- and 'H-NMR spectra reported in Fig. 6 experimental error 10
Publications Articles 1. Dinesh Mittal, Deepika Majithia, Richard Kennedy, Jamie Rhudy. "Differences in Characteristics and Outcome of Delirium Based on Referral Patterns." Psychosomatics, in press. 2. Richard E. Kennedy, Lee Livingston, Jennifer H. Marwitz, Shana Gueck, Jeffrey S. Kreutzer, Angelle M. Sander. "Complicated Mild Traumatic Brain Injury on the Inpatient Rehabilitation Unit: A Multi-Center Analysis." Journal of Head Trauma Rehabilitation, in press. 3. Richard E. Kennedy, Lee Livingston, Amy Riddick, Jennifer H. Marwitz, Jeffrey S. Kreutzer, Nathan D. Zasler. "Evaluation of the NFI as a Depression Screening Tool after Brain Injury." Journal of Head Trauma Rehabilitation, in press. 4. Janet P. Niemeier, Richard E. Kennedy, William O. McKinley, David X. Cifu. "The Loss Inventory: A Measure of Emotional and Cognitive Responses to Disability." Disability Rehabilitation, Vol. 26, No. 10, 2004. 5. Dinesh Mittal, Nita A. Jimerson, Emily P. Peoples, William D. Johnson, Richard E. Kennedy, Rafael A. Torres, Henry A. Nasrallah. "Risperidone in the Treatment of Delirium: Results from a Prospective Open-Label Trial." Journal of Clinical Psychiatry, Vol. 65, No. 5, 2004. 6. Richard Kennedy, Dinesh Mittal, Judith O'Jile. "Electroconvulsive Therapy in Movement Disorders: An Update." Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 15, No. 4, 2003. 7. Richard E. Kennedy, Risa N. Thompson, Todd G. Nick, Mark Sherer. "Use of the Cognitive Test for Delirium in Patients with Traumatic Brain Injury." Psychosomatics, Vol. 44, No. 4, 2003. 8. Anna Leung, Richard E. Kennedy, James L. Levenson. "Rabies Exposure and Psychosis." Psychosomatics, Vol. 44, No. 4, 2003. 9. Cynthia McGrath, Richard Kennedy, Wayne Hoye, Stuart Yablon. "Stereotypic Movement Disorder After Acquired Brain Injury: A Case Report." Brain Injury, Vol. 16, 2002. 10.Richard E. Kennedy, Derek M. Burnett, Brian D. Greenwald. "Use of Antiepileptics in Traumatic Brain Injury: A Review for Psychiatrists." Annals of Clinical Psychiatry, Vol. 13, No. 3, September 2001. 11.Dinesh Mittal, Judith O'Jile, Nita Jimerson, Richard Kennedy. "Trichotillomania Associated with Dementia: A Case Report." General Hospital Psychiatry, Vol. 23, 2001. 12.Rafael Torres, Dinesh Mittal, Richard Kennedy. "Use of Quetiapine in Delirium: Case Reports." Psychosomatics, Vol. 42, No. 4, July 2001. 13 rek M. Burnett, Richard E. Kennedy, David X. Cifu, and James Levenson. "Using Atypical Neuroleptic Drugs to Treat Agitation In Patients with a Brain Injury: A Review." Neurorehabilitation, Vol. 13, No. 3, 1999. 14. Richard Kennedy and James B. Hutchins. "Choline Acetyltransferase Expression Studied with an Oligonucleotide Probe." Cellular and Molecular Neurobiology, Vol. 12, No. 4, 1992. Book Chapters 1. Jesse R. Fann, Richard Kennedy, Charles Bombardier. "Physical Medicine and Rehabilitation." In Levenson JL. Essentials of Psychosomatic Medicine, American Psychiatric Press, in press. 2. Jesse R. Fann, Richard Kennedy, Charles H. Bombardier. "Physical Medicine and Rehabilitation." In Levenson JL. Textbook of Psychosomatic Medicine, 2004. 3. Paula T. Trzepacz and Richard E. Kennedy. "Delirium." In Silver JM, Yudofsky SC. Neuropsychiatry of Traumatic Brain Injury, 2nd Edition, 2004. Other Publications 1. Marisue Cody, Ellen Fisher, Cornelia Beck, and Richard Kennedy. Outcomes Module for Dementia OMD ; . Assisted with research and preliminary drafts of research module to be used in dementia outcomes studies. Abstracts 1. Richard Kennedy, Kellie J. Archer, Michael F. Miles. "Validation of the S-Score Algorithm in the Analysis of Gene Expression Data." [Abstract] Proceedings of the National Library of Medicine Informatics Training Conference 2005, Washington, DC. 2. Lee Livingston, Richard Kennedy, Jeffrey Kreutzer, Jennifer Marwitz, Angelle Sander. "Mild Traumatic Brain Injury on the Inpatient Rehabilitation Unit: A TBI Model Systems Analysis." Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 16, No. 2, Spring 2004. 3. Dinesh Mittal, Nita Jimerson, Emily Peoples, William Johnson, Richard Kennedy, Rafael Torres, Henry Nasrallah. "Treatment of Delirium with Risperidone: Results from an Open-Label Prospective Trial." Psychosomatics, Vol. 44, No. 2, March 2003 . 4. Richard Kennedy, Dinesh Mittal, Judith O'Jile. "Electroconvulsive Therapy in Movement Disorders: An Update." Psychosomatics, Vol. 43, No. 2, March 2002. 5. Richard Kennedy, Risa N. Thompson, Todd Nick, Mark Sherer. "Use of the Cognitive Test for Delirium in Traumatic Brain Injury." Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 14, No. 1, Winter 2002 and nadolol.
Polytropic murine viruses
Chemopreventive effects of a-naphthyl isothiocyanate xenobiotic-metabolizing enzymes and nitrosamine metabolism in rats. Carcinogenesis, 13, 2205--2210. Guo, Z., Smith, T.J., Wang, E., Eklind, K.L., Chung, F.-L. and Yang, C.S. 1993 ; Structure--activity relationships of arylalkyl isothiocyanates for the inhibition of 4- methylnitrosamino ; -1- 3-pyridyl ; -1-butanone metabolism and the modulation of xenobiotic-metabolizing enzymes in rats and mice. Carcinogenesis, 14, 1167--1173. Hecht, S.S. 1999 ; Chemoprevention of cancer by isothiocyanates, modifiers of carcinogen metabolism. J. Nutr., 129, 768S--774S. Heirwegh, K.P., Van de Vijver, M. and Fevery, J. 1972 ; Assay and properties of dititonin-activated bilirubin uridine diphosphate glucuronyltransferase from rat liver. Biochem. J., 129, 605--618. Hou, D.X., Fukuda, M., Fujii, M. and Fuke, Y. 2000 ; Transcriptional regulation of nicotinamide adenine dinucleotide phosphate: quinone oxidoreductase in murine hepatoma cells by 6- methylsufinyl ; hexyl isothiocyanate, an active principle of wasabi Eutrema wasabi Maxim ; . Cancer Lett., 161, 195--200. Huang, C., Ma, W.-Y, Li, J., Hecht, S.S. and Dong, Z. 1998 ; Essential role of p53 in phenethyl isothiocyanate-induced apoptosis. Cancer Res., 58, 4102--4106. Ino, N., Sugie, S., Ohnishi, M. and Mori, H. 1996 ; Lack of inhibitory effect of benzyl isothiocyanate on 5-b]pyridine PhIP ; -induced mammary carcinogenesis in rats. J. Toxicol. Sci., 21, 189--194. Isselbacher, K.J., Chrabas, M.F. and Quinn, R.C. 1962 ; The solubilization and partial purification of a glucuronyl transferase from rabbit liver microsomes. J. Biol. Chem., 237, 3033--3036. Ito, N., Matayoshi, K., Matsumura, K., Denda, A., Kani, T., Arai, M. and Makiura, S. 1974 ; Effect of various carcinogenic and non-carcinogenic substances on development of bladder tumors in rats induced by N-butylN- 4-hydroxybutyl ; nitrosamine. Jpn. J. Cancer Res., 65, 123--130. Ito, N., Hasegawa, R., Sano, M., Tamano, S., Esumi, H., Takayama, S. and Sugimura, T. 1991 ; A new colon and mammary carcinogen in cooked food, 5-b]pyridine PhIP ; . Carcinogenesis, 12, 1503--1506. Kaderlik, K.R., Minchin, R.F., Mulder, G.J., Ilett, K.F., Daugaard-Jenson, M., Teitel, C.H. and Kadlubar, F.F. 1994a ; Metabolic activation pathway for the formation of DNA adducts of the carcinogen 5-b]pyridine PhIP ; in rat extrahepatic tissues. Carcinogenesis, 15, 1703--1709. Kaderlik, K.R., Mulder, G.J., Shaddock, J.G., Casciano, D.A., Teitel, C.H. and Kadlubar, F.F. 1994b ; Effect of glutathione depletion and inhibition of glucuronidation and sulfation on 5-b] pyridine PhIP ; metabolism, PhIP--DNA adduct formation and unscheduled DNA synthesis in primary rat hepatocytes. Carcinogenesis, 15, 1711--1716. Kassie, F., Rabot, S., Uhl, M., Huber, W., Qin, H.M., Helma, C., Schulteu Hermann, R. and Knasmller, S. 2002 ; Chemopreventive effects of garden cress Lepidium sativum ; and its constituents toward 2-amino-3-methylimidazo[4, 5-f]quinoline IQ ; -induced genotoxic effects and colonic preneoplastic lesions. Carcinogenesis, 23, 1155--1161. Koide, A., Fuwa, K., Furukawa, F., Hirose, M., Nishikawa, A. and Mori, Y. 1999 ; Effect of cigarette smoke on the mutagenic activation of environmental carcinogens by rodent liver. Mutat. Res., 428, 165--176. Laemmli, U.K. 1970 ; Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature, 227, 680--685. Layton, D.W., Bogen, K.T., Knize, M.G., Hatch, F.T., Johnson, V.M. and Felton, J.S. 1995 ; Cancer risk of heterocyclic amines in cooked foods: an analysis and implications for research. Carcinogenesis, 16, 39--52. Leonard, T.B., Popp, J.A., Graichen, M.E. and Dent, J.G. 1981 ; aNaphthylisothiocyanate induced alterations in hepatic drug metabolizing enzymes and liver morphology: implications concerning anticarcinogenesis. Carcinogenesis, 2, 473--482. Liu, J.Z., Zhang, B.Z. and Milner, J.A. 1994 ; Dietary selenite modifies glutathione metabolism and 7, 12-dimethylbenz a ; anthracene conjugation in rats. J. Nutr., 124, 172--180. Long, D.J., II, Waikel, R.L., Wang, X.J., Roop, D.R. and Jaiswal, A.K. 2001 ; NAD P ; H: quinone oxidoreductase 1 deficiency and increased susceptibility to 7, carcinogenesis in mouse skin. J. Natl Cancer Inst., 93, 1166--1170. Makiura, S., Kamamoto, Y., Sugihara, S., Hirao, K., Hiasa, Y., Arai, M. and Ito, N. 1973 ; Effect of 1-naphthylisothiocyanate and 3-methylcholanthrene on hepatocarcinogenesis in rats treated with diethylnitrosamine. Gann, 64, 101--104. Manson, M.M., Ball, H.W.L., Barrett, M.C., Clark, H.C., Judah, D.J., Williamson, G. and Neal, G.E. 1997 ; Mechanism of action of dietary chemoprotective agents in rat liver: induction of phase I and II drug metabolizing enzymes and aflatoxin B1 metabolism. Carcinogenesis, 18, 1729--1738. Michaud, D.S., Spiegelman, D., Clinton, S.K., Rimm, E.B., Willett, W.C. and Giovannucci, E.L. 1999 ; Fruit and vegetable intake and incidence of bladder cancer in a male prospective cohort. J. Natl Cancer Inst., 91, 605--613. Misiewicz, I., Skupinska, K. and Kasprzycka-Guttman, T. 2003 ; Sulforaphane and 2-oxohexyl isothiocyanate induce cell growth arrest and apoptosis in L-1210 leukemia and ME-18 melanoma cells. Oncol. Rep., 10, 2045--2050. Mori, Y., Yamazaki, H., Toyoshi, K., Makino, T., Obara, T., Yokose, Y. and Konishi, Y. 1985 ; Mutagenic activation of carcinogenic N-nitrosopropylamines by rat liver: evidence for a cytochrome P-450 dependent reaction. Carcinogenesis, 6, 415--420. Mori, Y., Koide, A., Fuwa, K. and Kobayashi, Y. 2001 ; N-benzylimidazole for preparation of S9 fraction with multi-induction of metabolizing enzymes in short-term genotoxicity assays. Mutagenesis, 16, 479--486. Mori, Y., Koide, A., Kobayashi, K., Morimura, K., Kaneko, M. and Fukushima, S. 2002 ; Effect of ethanol treatment on metabolic activation and detoxification of esophagus carcinogenic N-nitrosamines in rat liver. Mutagenesis, 17, 251--256. Mori, Y., Koide, A., Kobayashi, Y., Furukawa, F., Hirose, M. and Nishikawa, A. 2003 ; Effects of cigarette smoke and a heterocyclic amine, MeIQx on cytochrome P-450, mutagenic activation of various carcinogens and glucuronidation in rat liver, Mutagenesis, 18, 87--93. 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Nowell, S.A., Massengill, J.S., Williams, S., Radominska-Pandya, A., Tephly, T.R., Cheng, Z., Strassburg, C.P., Tukey, R.H., MacLead, S.L., Lang, N.P. and Kadlubar, F.F. 1999 ; Glucuronidation of 5-b]pyridine by human microsomal UDPglucuronosyltransferases: identification of specific UGT1A family isoforms involved. Carcinogenesis, 20, 1107--1114. Sasaki, S. 1963 ; Inhibitory effects by alpha-naphthylisothiocyanate on development of hepatoma in rats treated with 30 -methyl-4dimethylaminoazobenzene. J. Nara Med. Assoc., 14, 101--115. Shirai, T., Sano, M., Tamano, S. Takahashi, S., Hirose, M., Futakuchi, M., Hasegawa, R., Imaida, K., Matsumoto, K., Wakabayashi, K., Sugiura, T. and Ito, N. 1997 ; The prostate: a target for carcinogenicity of 5-b]pyridine PhIP ; derived from cooked foods. Cancer Res., 57, 195--198. Sidransky, H., Ito, N. and Verney, E. 1966 ; Influence of a-naphthylisothiocyanate on liver tumorigenesis in rats ingesting ethionine and N-2fluorenylacetamide. J. 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Murine il-3
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ABSTRACT Poly ADP-ribose ; polymerase PARP ; knockout mice are resistant to murine models of human diseases such as cerebral and myocardial ischemia, traumatic brain injury, diabetes, Parkinsonism, endotoxic shock and arthritis, implicating PARP in the pathogenesis of these diseases. Potent selective PARP inhibitors are therefore being evaluated as novel therapeutic agents in the treatment of these diseases. Inhibition or depletion of PARP, however, increases genomic instability in cells exposed to genotoxic agents. We recently demonstrated the presence of a genomically unstable tetraploid population in PARP fibroblasts and its loss after stable transfection with PARP cDNA. To elucidate whether the genomic instability is attributable to PARP deficiency or lack of PARP activity, we investigated the effects of PARP inhibition on development of tetraploidy. Immortalized wild-type and PARP fibroblasts were exposed for 3 weeks to 20 M GPI 6150 1, 11b-dihydro-[2H]benzopyrano[4, ; , a novel small molecule specific competitive inhibitor of PARP Ki 60 nM ; and one of the most potent PARP inhibitors to date IC50 0.15 M ; . Although GPI 6150 initially decreased cell growth in wild-type cells, there was no effect on cell growth or viability after 24 h. GPI 6150 inhibited endogenous PARP activity in wild-type cells by 91%, to about the residual levels in PARP cells. Flow cytometric analysis of unsynchronized wild-type cells exposed for 3 weeks to GPI 6150 did not induce the development of tetraploidy, suggesting that, aside from its catalytic function, PARP may play other essential roles in the maintenance of genomic stability. INTRODUCTION PARP mice, with a homozygous disruption of the poly ADPribose ; polymerase PARP ; gene, do not express any PARP detectable by immunoblot analysis 1, 2 ; . They suffer far less tissue injury in murine models of a number of human diseases and nafcillin.
Identical at the nucleotide level to the same region in E. coli and contains nearly identical regions implicated in MarR and MarA binding 35, 37 ; . To better compare the operator promoter regions, we identified marRAB transcription start sites by primer extension, thereby empirically defining the promoter sites of both organisms. The start site for E. coli conforms to the expected site defined by putative 10 and 35 regions upstream of marRAB, originally identified by Cohen et al. 12 ; . The S. typhimurium promoter sites are similarly situated Fig. 2 ; . SAL-mediated induction of marRAB transcription appears identical in both organisms. By Northern blot analysis, SAL was shown to induce the accumulation of marRABSt mRNA Fig. 3 ; . Also, since treatment of E. coli mar mutants with tetracycline has been reported to elevate mRNA levels of both marRAB and the upstream marC 12 ; , it was possible that treatment with SAL would do the same. While induction of the upstream transcript by SAL was more pronounced in S. typhimurium than in E. coli, where little effect was observed, this induction was much smaller than that of the marRAB transcript Fig. 3 ; . The similarity to E. coli of nucleotide sequences of the operator promoter regions, Northern data on inducibility of the operon by SAL, and structural and functional similarities of MarR to its E. coli counterpart all suggests that regulated control of marRAB expression in S. typhimurium is nearly identical to that of E. coli. When grown in the presence of SAL or when containing plasmids expressing MarAEc, S. typhimurium strains that are capable of infection in BALB c mice were less susceptible to different classes of antibiotics than were less virulent S. typhimurium and E. coli strains Table 2 ; . This finding suggested a possible correlation between MarA-mediated antibiotic resistance and virulence potential. Therefore, the contribution of marA in virulence was assessed by using a well-established murine model of infection 24 ; . However, the S. typhimurium marA strain did not differ from the wild-type control in the level of killing of BALB c mice. We note that our LD50s were much lower than those reported for an isogenic gyrA 1816 strain 24 however, this difference does not affect the result since our two strains exhibited indistinguishable LD50s. Thus, we could not implicate marA in S. typhimurium virulence. If marA is involved in virulence, it is possible that its effect is masked by the activation of other overlapping regulons that engender a phenotypic antibiotic resistance. Some of the genes controlled by marRAB are also members of the redox-sensitive soxRS regulon 2, 22 ; in which constitutive mutations also confer a Mar phenotype 23, 39 ; . The regulatory overlap is presumably due to the strong homology between the direct activators of both regulons, SoxS and MarA 12 ; . The soxRS regulon protects the cell against both redox-cycling compounds 43, 55 ; and the nitric oxide free radical NO ; 41, 42 ; , as well as NO -generating activated macrophages 41, 42 ; . Thus, some genes common to both the marRAB and soxRS regulons are likely to be expressed in vivo, as a consequence of soxRS activation. marRAB may therefore be redundant when S. typhimurium is in contact with macrophages, where it is known to escape humoral defenses 18 ; . In addition, recent evidence indicates that overexpression of another MarA homolog, Rob, also results in multiple antibiotic resistance 3 ; , presumably by activating promoters common to the MarA regulon. Experiments designed to evaluate strains containing combinations of marRAB, soxRS, and rob mutations for attenuation of virulence may identify overlapping roles for these genes in pathogenesis. Studies focusing on MarA-regulated intrinsic antibiotic resistance can now be conducted in two different organisms. Although the natural physiological role of the two operons is.
Generation of murine dendritic cells
Seregi A, Keller M & Hertting G 1987 ; . Are cerebral prostanoids of astroglial origin? Studies on the prostanoid forming system in developing rat brain and primary cultures of rat astrocytes. Brain Res 404, 113120. Smith SJ 1994 ; . Neural signalling. Neuromodulatory astrocytes. Curr Biol 4, 807810. Vitadello M & Denis-Donini S 1990 ; . Expression of neurofilament proteins in granule cells of the cerebellum. Brain Res 509, 4754. Williams A, Van Dam AM, Ritchie D, Eikelenboom P & Fraser H 1997 ; . Immunocytochemical appearance of cytokines, prostaglandin E2 and lipocortin-1 in the CNS during the incubation period of murine scrapie correlates with progressive PrP accumulations. Brain Res 754, 171180. Yasojima K, Tourtellotte WW, McGeer EG & McGeer PL 2001 ; . Marked increase in cyclooxygenase-2 in ALS spinal cord: implications for therapy. Neurology 57, 952956. Zonta M, Angulo MC, Gobbo S, Rosengarten B, Hossmann KA, Pozzan T & Carmignoto G 2003 ; . Neuron-to-astrocyte signaling is central to the dynamic control of brain microcirculation. Nat Neurosci 6, 4350 and naloxone
Parental Armstrong virus. By contrast, staining with NLDC 145, an antibody which recognizes a subpopulation of longlived splenic dendritic cells the interdigitating cells in the central periarterial sheaths [12, 30] ; , revealed a substantial loss of these cells from spleens of mice infected with clone 13 Fig. 1c and higher-power pictures in Fig. 2 ; . Although mice infected with LCMV Armstrong are undergoing an immune response with associated activation-induced changes in the spleen, NLDC 145-positive cells were clearly present within the white pulp Fig. 2B ; . In clone 13-infected mice, however, NLDC 145-positive cells were completely lost from much of the white pulp, and the PALS in these areas appeared morphologically to have disintegrated Fig. 2C ; . As the organization of both the T- and B-cell areas of the PALS was destroyed, likely not only NLDC 145-positive periarterial interdigitating dendritic cells in the T-cell areas but also follicular dendritic cells in the B-cell areas were depleted in clone 13-infected mice. Figure 1c illustrates that NLDC 145-positive cell depletion was not absolute. These cells remained and the architecture was retained in 10 to 50% of the PALS areas in the sections examined. Loss of periarterial interdigitating dendritic cells from the white pulp in the spleens of clone 13-infected mice was confirmed by staining with N418, an antibody to murine CD11c. In the steady state in the spleen, the main cells expressing high levels of CD11c are dendritic cells--both the NLDC 145-positive subpopulation of interdigitating cells in the central periarterial sheaths and the more short-lived population of dendritic cells which lie in the periphery of the T-cell area interrupting the marginal zone of macrophages 61 ; . Both periarterial and peripheral N418-positive cells were present in Armstrong-infected mice, whereas in clone 13-infected mice there was a loss of periarterial N418 staining Fig. 1 ; . The N418-positive cells in the marginal zone and red pulp of clone 13-infected mice may be peripheral dendritic cells or other cell types such as macrophages on which CD11c can be upregulated during an immune response. Loss of interdigitating periarterial dendritic cells from clone 13-infected mice is CD8-dependent and clone 13-infected mice mount a short-lived antiviral CTL response at early times postinfection. Further experiments investigated the mechanism by which interdigitating periarterial dendritic cells are depleted following infection of mice with LCMV clone 13. First, it was shown that dendritic cell loss was CD8 dependent, as in vivo depletion of CD8 T cells using a subset-specific monoclonal antibody prior to infection of mice with LCMV clone 13 prevented the NLDC 145-positive cell loss and associated disintegration of the PALS which occurred in undepleted mice Fig. 1d and 2D ; . As the LCMV-specific CTL response is mediated by CD8 T cells reviewed in reference 46 ; , this finding raised the question of whether the CD8 dependent immunopathological damage might be mediated by virus-specific CTL. The immunosuppressive clone 13 LCMV variant was initially characterized as a virus which is able to establish a persistent infection in adult immunocompetent mice because the CTL response generated to it is insufficient to achieve viral clearance 2 ; . Indeed, 7 days postinfection when the CTL response to LCMV Armstrong peaks, only low levels of LCMV-specific CTL activity are detected in clone 13-in and murine.
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